To round out the year, here are three tutorials on the blood gas machine, blood gas analysis and the blood gas printout.
The first tutorial looks at how oxygen is measured using the Clark Electrode on the blood gas analyser and demonstrates the importance of co-oximetry in modern blood analysis. From that the fractional saturation of hemoglobin with oxygen is derived.
The second tutorial explains the Glass Electrode that measures pH and PCO2. Subsequently I cover problems you might encounter with blood gas sampling. If you don’t want to watch the technical stuff, I strongly recommend you scroll to the middle of the tutorial (12 minutes in) as it covers information that all healthcare practitioners must know.
The final tutorial looks at all of that other data that appears on blood gas printouts that you may never have understood – and it can be really confusing – DERIVED or calculated variables (bicarbonate, temperature correction, TCO2, O2 content, Base Excess, Standard Bicarbonate, Anion Gap etc.). I cover both the Radiometer ABL machines and the GEM 5000. I guarantee you’ll learn something.
As part of my fundamentals of Anesthesiology and Critical Care Series I have posted 3 tutorials on the Role of CO2 /HCO3 in Acid Base Balance. These are entirely new tutorials (not part of the previous acid base series – that I have not finished yet! There is some overlap and updated facts and figures) and I have put a lot of work into getting the message of why the respiratory system is so important in acid base. Tutorial 1 is the basics of acid base. Tutorial 2 discusses respiratory acidosis, acute and chronic, and respiratory alkalosis. Tutorial 3 discusses respiratory compensation for acute metabolic acidosis. Although I cover the respiratory component in great depth, I also explain what metabolic acidosis is, what causes it and briefly discuss the anion gap, expected bicarbonate, base deficit and base deficit gap. I guarantee that you will learn something.
Traditionally rules of thumb regarding the changes in PaCO2 and Bicarbonate in acid base balance have utilized mmHg. Unfortunately, in large tracts of the world, particularly in Europe, blood gases are reported in the SI unit kPa. This tutorial is for those people. I cover various acid base abnormalities – pH vs PaCO2, acute and chronic respiratory acidosis, respiratory alkalosis, metabolic acidosis and alkalosis and go through the various acid base rules of thumb using kPa, with examples. I guarantee you’ll learn something.
Rules:
Rule 1 H+ vs pH: a 1nmol/L increase in [H+} results in a 0.01 fall in pH
Rule 2 PaCO2 in Apnea: In apnea the PaCO2 rises by 1.5kPa in the first minute and by 0.5kPa per minute thereafter (this reduces progressively over time to 0.2-3kPa)
Rule 3 PaCO2 vs pH: For every 1kPa increase in the PaCO2 the pH falls by 0.06
Rule 4 PaCO2 vs HCO3 in Acute Respiratory Failure: For every 1kPa increase in the PaCO2, the HCO3 rises by 1mmol/L
Rule 5 PaCO2 vs HCO3 in Chronic Respiratory Failure: For every 1kPa increase in the PaCO2, the HCO3 rises by 3mmol/L and the Chloride falls by an equal value.
Rule 6 PaCO2 vs HCO3 in Acute Respiratory Alkalosis: For every 1kPa increase in the PaCO2, the HCO3 falls by 2mmol/L
Rule 7 PaCO2 versus Base Deficit in Acute Metabolic Acidosis: For every 1mmol/L increase in the Base Deficit (-BE e.g. from -1 to -2), the PaCO2 falls by 0.13kPa e.g. if the BD is -10 the PaCO2 will fall by 1.3kPa from 5.3 to 4
Rule 8 PaCO2 vs HCO3 in Chronic Metabolic Alkalosis (in ICU): For every 1mmol/L increase in the Base Excess (or HCO3) the PaCO2 increase by 0.13kPa e.g. if the BE is +10 then the PaCO2 will increase from 5.3 to 6.6
This is Tutorial 4 in the Acid Base Series – on the topic of Metabolic Acidosis. The tutorial is based on a single blood gas – a random sample that was handed to me in the ICU recently. Blood Gas Used in This Tutorial: pH 7.19 PaCO2 32mmHg (4.1kPa) HCO3- 13.1 BE – 16.5 AG 20 Na+ 126 K+ 3.1 Cl- 96 Lactate- 7.2 Ketones- 0.6mmol/L Albumin 21g/L Creatinine 3.3mg/dl (293mmol/l)
Metabolic Acidosis is characterized by an increase in the relative ratio of strong anions to strong cations in the plasma. The PaCO2 and the Bicarbonate fall in a predictable manner. It is possible to compute the effectiveness of respiratory compensation for metabolic acidosis by using the Winters equation.
To understand the mechanism of metabolic acidosis – caused by accumulation of mineral (Chloride) and organic (Lactate, Ketones, Metabolic Junk Products) anions – one needs to apply the law of Electrical Neutrality. All of the positive charges must equal all of the negative charges. As Bicarbonate is consumed in the process of buffering metabolic acidosis, the change in the Bicarbonate level (downwards) can be used to quantify the degree of acidosis. This is important because the pH may be within the normal range due to respiratory compensation. Be aware that the HCO3- quantum that is displayed on a blood gas is derived from the pH and PCO2 by the Henderson Hasselbalch equation.
Unfortunately, because respiratory abnormalities may complicate the diagnosis of metabolic acidosis, and pH and PCO2 are altered by changes in temperature, the precision of a single reading of PCO2 and HCO3- may be poor. Consequently, the Standard Base Excess was developed to excise the respiratory component from the change in bicarbonate. Again it is a derived variable and may be imprecise. Nevertheless, BE (or 1-BE the Base Deficit BD) is a terrific scanning tool to identify the presence of a metabolic acidosis (BD) or alkalosis (BE). It is defined as the amount of strong cation (BD) or strong anion (BE) required to bring the pH back to 7.4 when the temperature is 37 degrees Celcius and the the PaCO2 is 40mmHg or 5.3kPa.
The Base Deficit does not indicate the source of the acidosis, but it can be recalculated to remove the impact of the [Na+], the [Cl-], the body water and the serum Albumin (and the Lactate) to determine the Base Deficit Gap – indicative of the quantity of Unmeasured Anions (UMA, Ketones, if not measured, and Renal Acids (metabolic junk products – MJP).
Traditionally clinicians use the Anion Gap to determine whether a patient has a Hyperchloremic Acidosis (no gap) from a UMA acidosis. I find this quite a dated concept. If the [Cl-] exceeds 105 and the plasma Sodium is normal, the patient has a Hypercloremic acidosis. We can easily measure Ketones and Lactate. The AG is imprecise and should be adjusted for the Albumin level, which tends to hover around 25g per liter in critically ill patients (narrowing the Gap and alkalinizing the patient). I do think if you are calculating the AG that you must include the K+ on the Cation side, the Lactate on the Anion side and adjust the Albumin.
The Strong Ion Gap is a more advanced, more precise and more cumbersome version of the AG. Regardless of the approach, one eventually ends up with a quantify of unidentifiable anions (SIG) that may be of medley origin (metabolism, poisoning etc). It is my opinion that it is useful to tease out all of the different acidifying and alkalinizing processes (the Fencl approach) to determine what is going on with the patient. All of these calculations can be done in seconds with smartphone apps and spreadsheets.
ORtoICU 